We tried functional cloning to find new molecules controlling the response of nucleic acid-sensing Toll-like receptors (TLRs), like TLR7. As the other way, we analyzed the phenotype of Unc93 homolog B1 (Unc93B1) D34A mutant mice, which suffer from systemic inflammation caused by TLR7 hyperactivationAs results, we found that the phenotype of D34A mice was attenuated by lacking type I interferon receptor (IFNAR1). Type I IFN signaling maintained the expression of TLR7 in B cells, and the number of TLR7-expressing conventional dendritic cells, respectively.